Poorly understood, but may be defects in both cell mediated and humoral immunity (possible genetic trigger)

Hypergammaglobulinemia

Possible Infectious trigger

Possible Medications: may be association with NSAID or Antibiotic exposure

CLINICAL PEARL: TINU may be difficult to distinguish from other systemic diseases, i.e. Sarcoidosis, Sjögren's Syndrome, systemic lupus erythematosis (SLE) , Tuberculosis or Behçet's Disease, but in these disorders, interstitial nephritis is less common as a renal manifestation and typically presents as proliferative glomerulonephritis, secondary amyloidosis or vasculitis.

Renal Biopsy

Interstitial inflammation with lymphocyte predominance

Interstitial eosinophils ± neutrophils may be seen (30%)

Non-caseating granulomas

Immunofluoresecence is typically negative

Prognosis

Ocular complications = good in ~ 75% of patients

No long term studies to characterize follow-up of nephritis

Treatment

May resolve spontaneously or after discontinuation of inciting medications

(One of the first retrospective studies to document the clinical, laboratory and histological features of AIN and compare patients treated with Corticosteroids versus those managed conservatively. 42 patients (26 managed conservatively and 16 treated with corticosteroids) were followed for 1 year and there was NO discernible difference in outcome.Strengths of the study: ALL patients had biopsy proven AIN and they were similarly matched groups both clinically and histologically (interestingly, the steroid treated group had a LOWER serum creatine versus the conservatively managed, 6.2mg/dL versus 7.9 mg/dL)Limitations of this study: small number of patients, majority (44%) were related to NSAIDs and only 60% received corticosteroids.)

(A detailed review article that summarizes the presentation and management of AIN. It includes a table of frequent drug associated causes of AIN and reviews the sensitivity and specificity of eosinophiluria in the diagnosis of AIN.)